Abstract
Background: Traditional risk factors for atherosclerotic disease (AD) are well-known, of which some are relevant also for abdominal aortic aneurysms (AAA). The present study compares the importance of plasma biomarkers and traditional risk factor profiles for incident AD without concomitant AAA (isolated AD) and AAA without concomitant AD (isolated AAA) during long-term follow-up.Methods: In the Malmö Diet and Cancer Study—cardiovascular cohort, 5,381 participants were free from atrial fibrillation or flutter, AD (coronary artery disease, atherothrombotic ischemic stroke, carotid artery disease, or peripheral artery disease), and AAA underwent blood sampling under standardized fasting conditions between 1991 and 1994. Cox proportional hazards regression analysis was used to calculate hazard ratios (HR) with 95% CIs.Results: During a median follow-up of 23.1 years, 1,152 participants developed isolated AD, and 44 developed isolated AAA. Adjusted HR for lipoprotein-associated phospholipase A2 (mass) (HR 1.53, 95% CI 1.14–2.04 vs. HR 1.05, 95% CI.99–1.12) was higher for incident isolated AAA compared to incident isolated AD, respectively. Mid-regional pro-adrenomedullin (MR-proADM) was associated with incident isolated AD (HR 1.17, 95% CI 1.1–1.25) and incident isolated AAA (HR 1.47, 95% CI 1.15–1.88). MR-proADM was correlated (r = 0.32; p < 0.001) to body mass index (BMI), and BMI was associated with increased risk of incident isolated AAA (HR 1.43, 95% CI 1.02–2). No participant with diabetes mellitus (DM) at baseline developed isolated AAA (0/44), whereas DM was associated with an increased risk of isolated AD (HR 2.57, 95% CI 2.08–3.18). Adjusted HR for male sex (HR 4.8, 95% CI 2.42–9.48, vs. HR 1.76, 95% CI 1.56–1.98) and current smoking (HR 4.79, 95% CI 2.42–9.47 vs. HR 1.97, 95% CI 1.73–2.23) were higher in the incident isolated AAA group compared to the incident isolated AD group, respectively.Conclusions: The data supports the view that components of vascular inflammation and cardiovascular stress drives AAA development, whereas glycated cross-links in abdominal aortic wall tissue may have a plausible role in reducing AAA risk in individuals with DM.
Highlights
Atherosclerotic disease (AD) is the main leading cause of death in the world due to coronary and cerebral artery disease [1]
The above-mentioned plasma biomarkers have previously been analyzed in relation to incident cardiovascular disease in the same cohort [19], but to enhance the current understanding of the importance of plasma biomarker profiles for the development of either AD or Abdominal aortic aneurysm (AAA), it is of great interest to analyze plasma biomarker profiles in patients that either exclusively develops incident AD or incident AAA, extending the follow-up period for outcomes with 11 years resulting in a substantially increased number of both atherosclerotic and AAA events
Among the 1,196 patients, the first AD event was caused by coronary artery disease (n = 537; 44.9%), atherothrombotic ischemic stroke (n = 405; 33.9%), carotid artery disease (n = 89; 7.4%), and peripheral artery disease (n = 165; 13.8%)
Summary
Atherosclerotic disease (AD) is the main leading cause of death in the world due to coronary and cerebral artery disease [1]. The hemodynamic plasma biomarker B-type natriuretic peptide has been associated with both an early subclinical development of peripheral [15] and carotid [16] artery disease and AAA [17] decades before clinical manifestation in individuals free from disease. A biomarker of neurohormonal activation, mid-regional-pro-adrenomedullin (MR-proADM), has been associated with the prediction of both carotid artery disease [16] and AAA [18]. It appears that these biomarkers reflect the early onset of cardiovascular disease, reacting to either slow development of peripheral arterial atherosclerotic stenosis and/or abdominal aortic wall degeneration and aneurysm development. The present study compares the importance of plasma biomarkers and traditional risk factor profiles for incident AD without concomitant AAA (isolated AD) and AAA without concomitant AD (isolated AAA) during long-term follow-up
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